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Abstract

Recent investigations in animal ears have described temporary noise-induced hearing loss with permanent deafferentation for up to 50% of auditory nerve fibers in the high-frequency region of the cochlea (Kujawa and Liberman, 2009; Lin et al., 2011, Furman et al., 2013). Although thresholds remained normal, evidence of the deafferentation was apparent in reduced wave I auditory brainstem response (ABR) amplitudes for high-level stimuli. It is unknown if the same phenomenon exists in the human ear. The goal of this research project was to characterize cochlear and auditory nerve function in human ears with normal behavioral thresholds that are regularly and voluntarily exposed to high levels of noise. Data were collected from 30 normal-hearing subjects with different voluntary noise-exposure backgrounds. Auditory function was assessed across a range of stimulus levels via the ABR and distortion-product otoacoustic emissions (DPOAEs). ABRs were collected in response to 1 and 4 kHz tone bursts and a click stimulus. DPOAEs were assessed at 1, 2 and 4 kHz. Significantly smaller amplitudes were seen in wave I of the ABR in response to high-level (e.g., 70 to 90 dB nHL) click and 4 kHz tone bursts in ears with greater noise-exposure backgrounds. There were no statistically significant differences in supra-threshold DPOAE level across ears with different noise-exposure histories. These findings are consistent with data from previous work completed in animals where the reduction in high-level wave I ABR responses was a result of deafferentation of high-threshold/low-spontaneous rate auditory nerve fibers. These data suggest a similar mechanism may be operating in human ears following exposure to high sound levels. Furthermore, data from the present study suggest noise-induced auditory damage in normal-hearing ears is only apparent when examining supra-threshold ABR responses.